Polycystic ovary syndrome: a major unrecognized cardiovascular risk factor in women

Abstract

The prevalence of polycystic ovary syndrome (PCOS) is estimated to be nearly 10% among reproductive-age women. PCOS may represent the largest underappreciated segment of the female population at risk of cardiovascular disease. Clinicians providing care to women of childbearing age must recognize the presenting clues, including irregular menses, hirsutism, alopecia, hyperandrogenemia, and obesity. The pathophysiology of PCOS is complex, involving the hypothalamus-pituitary-ovarian axis, ovarian theca cell hyperplasia, hyperinsulinemia, and a multitude of other cytokine- and adipocyte-driven factors. Cardiac risk factors associated with PCOS have public health implications and should drive early screening and intervention measures. There are no consensus guidelines regarding screening for cardiovascular disease in patients with PCOS. Fasting lipid profiles and glucose examinations should be performed regularly. Carotid intimal medial thickness examinations should begin at age 30 years, and coronary calcium screening should begin at age 45 years. Treatment of the associated cardiovascular risk factors, including insulin resistance, hypertension, and dyslipidemia, should be incorporated into the routine PCOS patient wellness care program.

Keywords: Cardiovascular disease; Carotid intimal medial thickness; Coronary calcium screening; Diabetes; Obesity; Polycystic ovary syndrome.

Figure 1

Enlarged ovaries in a woman with polycystic ovary syndrome. (Photograph by Carolyn J. Alexander, MD.)

Figure 2

During the follicular phase of the menstrual cycle, ovarian theca cells respond to the luteinizing hormone (LH) by increasing androgenic precursor output. Follicle-stimulating hormone (FSH) stimulates granulose cells to aromatize androgens into estrogens, which ultimately end up in the blood stream. cAMP, cyclic adenosine monophosphate. Reprinted with permission from Speroff L and Fritz MA.

Figure 3

Insulin resistance leads to hepatic overproduction of apoB and VLDL (which ultimately leads to hypertriglyceridemia). HDL, high-density lipoprotein; LDL, low-density lipoprotein; LDLR, low-density lipoprotein receptor; ER, estrogen receptor; AR, androgen receptor; VLDL, very low-density lipoprotein; SR-B1, scavenger receptor B1; LPL, lipoprotein lipase; ApoB, apolipoprotein B; MTP, microsomal triglyceride protein; HL, hepatic lipase; FFA, free fatty acid; ERK ½ MAPK, extracellular signal regulated kinase ½ mitogen-activated protein kinase; PKA-HSL, protein kinase A hormone sensitive lipase complex. Reprinted from TRENDS in Endocrinology and Metabolism, Volume 18, Diamanti-Kandarakis E et al. Pathophysiology and types of dyslipidemia in PCOS. Pages 288–285. Copyright © 2007, with permission from Elsevier.

Figure 4

Patients with PCOS have an increased prevalence (> 4 times) of elevated C-reactive protein levels (> 5 mg/L). PCOS, polycystic ovary syndrome. Reprinted with permission from Boulman N et al.

Figure 5

Shown here are 12 ovarian cysts of 2 mm to 5 mm in diameter spanning the perimeter of the left and right ovaries. Reprinted from Balen AH et al. Ultrasound assessment of the polycystic ovary: international consensus definitions. Human Reproduction Update. 2003;9(6):505–514, by permission of the European Society of Human Reproduction and Embryology.